The present accepted theory of isoimmunization in pregnancy as the cause of congenital hemolytic disease does not explain the manifold clinical manifestations; nor why in the majority of cases no abnormal isoagglutinins can be detected in the maternal serum; nor why in some cases where the maternal serum contains potent agglutinins, the infant is perfectly normal though its red cells contain the specific agglutinogen. These puzzles have been solved by the discovery, , that individuals sensitized to agglutinogens such as Rh, Hr, A, B, etc., may form 2 sorts of antibodies, namely, agglutinins (bivalent antibodies) and/or blocking antibodies or glutinins (univalent antibodies). The clinical manifestations depend on the type of isoantibody present in the maternal serum, so according to the present writer's theory erythroblastosis fetalis comprises 2 disease syndromes instead of only one. The characteristics of these disease syndromes and the author's proposed terminology are as follows: (1) Congenital hemolytic disease. This syndrome is caused by the presence in the maternal serum of univalent antibodies specific for the fetal red cells. When only small amounts of antibody get into the fetal circulation, the infant is born alive, but develops an anemia which readily responds to proper transfusion therapy. When larger amounts are present in the maternal serum, so that more passes into the fetus, the process progresses further in utero until the degree of anemia is such that anoxemia of the capillary walls permits exudation of serum proteins into the tissue spaces. A stillbirth results, or a living infant with hydrops, an almost invariably fatal condition. In these “pale” cases the characteristic pathological findings are marked pallor, ascites, anasarca, splenomegaly, hepatomegaly, and microscopically extramedullary islands of hematopoiesis in the liver and spleen and hemosiderosis of the liver and spleen. (2) Erythroblastosis proper. Since agglutinins are presumably larger molecules than blocking antibodies, these only rarely traverse the placenta during pregnancy. During labor and delivery, however, increased intrauterine pressure may milk agglutinins into the fetal circulation.